The ordered map or the body in the CNS is thoght to depend upon an equally oredered primary afferent inneration of the brainstem during development. While there is strong evidence for this view, the hypothesis guiding the proposed experiments is that somatotopically ordered primary afferents are insufficient for the maintenance of normal central representations. This proposal was prompted by the observation that transection of the infraorbital nerve (ION) or cauterization of a single row of vibrissae follicles in newborn rats and staining of brainstem sections 2 to 10 days later with an antibody directed against galanin reveals a somatotopically organized pattern which corresponds to the portion of the periphery that would be represented by teh damaged primary afferents. Our as yet unproven assumption is that the galanin-positive fibers are the central arbors of priamry afferents that survived peripheral axotomy. We will test this proposal and the above-stated hypothesis by answering the following questions; 1) Is the vibrissae-related galanin immunoreactivity in the trigeminal (V) brainstem complex of perinatal rats that have sustained neonatal vibrissae follicle or ION damage located in primary afferent axons? We will determine whether or not this is the case in two types of experiments. First, if the galanin immunoreactivity is in application of Di-I in fixed tissue. 2) Does neonatal ION damage alter the aggregation of V brainstem neurons during the period when primary afferents are still somatotopically organized? Our working hypothesis would suggest that vibrissae-related clusterin of PrV neurons and their dendrites will be lost while primary afferents are still ordered. We will test this by retrograde tracing and intracellular labelling experiments. 3) What is the primary afferent "signal" required for the maintenance of central somatotopy during early postnatal life. Results from both our own and other laboratories suggest that some factor conveyed from the periphery other than NGF is necessary to maintain the clustering of second order V cells and somatotopic patterns in higher center. We will test this hypothesis by blocking axoplasmic transport in the developing ION and assessing the organization of primary afferent axon arbors and central V patterns using the methods outlined above. 4) Do the abnormal central arbors of damaged V primary afferetns observed at long intervals after transection result from abnormalities in peripheral regeneration? Our hypothesis is that loss of contact with the periphery does not substantially alter the central arbors of V primary afferents. However, examination of single axons at long intervals after peripheral damage demonstrates clear morphological changes. We believe that these changes are associated with abnormalities in peripheral regeneration and will test this view by transecting ION axons, preventing their regeneration, and filling them with HRP 2 to 3 months after transection.